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Proceedings of the Royal Society of Medicine

W. G. FEGAN, M.Ch. F.R.C.S.I.

I hope this paper will stimulate some surgeons to reconsider the treatment of varicose veins and to give a trial to the treatment I describe. Its simplicity is deceptive.

It is by means easy to put on a bandage just so tightly and no more, to have it stay on without interruption for six weeks, to persuade a patient to walk three miles or more per day and to convince him or her of the importance of not standing. One must also avoid loosening or wrinkling of the bandage. All these minor points have to be watched carefully to achieve the ideal result.

Too much attention is paid to the eradication of the superficial varices; too little to the restoration of the efficiency of the multiple pumping units beneath the deep fascia of the leg. Superficial varices disappear spontaneously following the occlusion of a leak from one of the pumps. It is unnecessary to strip out the entire superficial dilated vein in order to restore normality. Advantage is not taken of the fact that veins are capable of returning to normal after the abnormal influence to which they are exposed is corrected. Obstetricians regularly tell us of the incredible degree of recovery in bad varices following delivery. All our attention should be directed towards the restoration of pumps rather than the eradication of the superficial varices by stripping; most stripped veins have good valves and have walls capable of recovering their original condition. Also it may well be that one day these veins may be needed by the patient for arterial surgery.

Derangements of the venous pumps are due to valvular incompetence. We distinguish between primary and secondary incompetence: by primary incompetence we refer to those destroyed valves, the cusps of which have become fouled by thrombosis and recanalization; this is the common cause of leakage through the perforating veins. Secondary incompetence develops with the gradual dilitation of the superficial vein in an upward direction from the site of such a leak; it is reversible because the valve cusps are still normal and have not been permanently damaged; the only abnormality lies in stretching of the valvular ring and this will recover soon after the incompetent perforating vein has been destroyed. Secondary incompetence, in contradistinction to primary, is reversible and greater advantage should be taken of this reversibility in the treatment of varicose veins.

The reserve pumping capacity of the multiple pumping units in the leg, foot and thigh is far in excess of that normally required, and it is only when this reserve efficiency has been dissipated by leakage that symptoms appear. Not until damage is excessive or occurs at a particular strategic vein (such as the ankle perforator) does failure of the system become clinically apparent. Injury to one or two valves in a person with many valves is frequently symptomless. The reserve is largely proportional to the number of valves in the pump. A system with few valves has a poor reserve efficiency. Treatment should be aimed at restoring as much as possible of this reserve pumping power.

Widespread thrombosis with recanalization of veins and destruction of valves followed the old form of sclerotherapy, and produced a group of patients with chronic venous insufficiency more serious than before they began treatment. This was not generally appreciated on account of temporary improvement following the treatment and prior to thrombus recanalization. If re-opening of the thrombosed section of vein and damage to good valves can be avoided, then sclerotherapy can be a satisfactory form of treatment.

The following technique is designed to these ends, producing minimal injury to normal, or potentially normal valves, and developing a permanent barrier to the retrograde flow of blood from the deep into the superficial veins. Following selection of an injection site (i.e. the segment of superficial vein opposite an incompetent perforating vein), 0.5 ml sodium tetradecyl is introduced into this segment, which has previously been emptied of blood by elevation of the limb (Fig. 1). The segment is isolated for about one minute by finger compression above and below the point of injection, thus allowing concentrated sclerosant to have maximal effect upon the isolated segment of vein wall (Fig. 2). Crepe bandages are then applied both above and below the injected segment, and a rubber pad is placed over the site, and bandaging completed (Fig. 3).

Other incompetent perforating veins should be similarly injected at the same session, and the limb is finally bandaged from the webs of the toes up to above the highest injection site. A full-length, two-way-stretch elastic stocking is then worn over the bandages, day and night, the stocking being held by a suspender belt to prevent it from rolling down; this also should be worn at night. The patient is instructed to walk at least three miles every day and to avoid standing. The avoidance of standing is particularly important in the production of good results. Compression must be maintained for at least six weeks after the last perforator has been injected, or until the clinical end-point is achieved. Otherwise, the vein will reopen, become painful and tender, and reproduce the florid thrombophlebitis which brought discredit upon the old form of sclerotherapy. If on the other hand compression is adequately maintained, the ideal end-result of a short cord-like segment of painless fibrotic vein is achieved. This is a satisfactory clinical end-point after which compression can safely be removed. Not until the treated vein ceases to be tender on palpation is it safe to remove the compression. Occasionally the segment is still tender after six to eight weeks compression; in such cases further investigation will often reveal the presence of a still undiagnosed incompetent perforating vein near the site.

The prevention of reopening is the principal objective of our treatment. The reasons fore opening of veins after thrombosis are as follows: (1) Retraction of the clot to the side of the lumen to which it is most firmly attached. (2) The water-hammer effect of the blood in the unthrombosed segment of vein which gouges a line of cleavage between the reacting thrombus and the weakened vein wall. (3) The natural tendency of the normal lining of the vein wall to proliferate and split, forming sinuses which soon establish connection with the venous system.

If compression is applied immediately following injection and maintained, the histological and clinical picture is very different: (1) The large thrombus which plugged the vein is reduced to the minimum. (2) The vein wall is greatly thickened relative to the size of the thrombus, i.e. the wall-thrombus ration is reversed. (3) The invasion of the small amount of thrombus in the lumen is much more aggressive and its organization completed much more rapidly. (4) The development of peripheral sinuses does not take place. (5) The firm union which is developed rapidly between wall and thrombus can withstand the water-hammer effect of the blood in the unthrombosed section.

Histological studies of a large number of biopsies from veins which have been treated by us over a five-year period show that the fibrosis developed in the wall of the thickened vein is fused with the organized thrombus and remains as a permanent barrier (Fig. 4).

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